Patent application number | Description | Published |
20080214452 | METHOD FOR EFFECTING LOCALIZED, NON-SYSTEMIC AND SYSTEMIC, IMMUNOGENIC TREATMENT OF CANCER USING CRT TRANSLOCATION - Anthracyclines-treated tumor cells are particularly effective in eliciting an anti-cancer immune response, where the rDNA-damaging agents, such as etoposide and mitomycin C do not induce immunogenic cell death. Anthracyclines induce the rapid, pre-apoptotic translocation of calreticulin (CRT) to the cell surface. Blockade or knock down of CRT suppressed the phagocytosis of anthracyclines-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. The anthracyclines-induced CRT translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex. Administration of recombinant CRT or inhibitors of protein phosphatase1/GADD34 restored the immunogenicity of cell death elicited by etoposide and mitomycin C, and enhanced their antitumor effects in vivo. These data identify CRT as a key feature determining anti-cancer immune responses and delineate a possible strategy for immunogenic chemotherapy. | 09-04-2008 |
20090004134 | KIT FOR TREATING A HEALTH CONDITION BY INDUCING TRANSLOCATION OF AN ERP57 PROTEIN TO A CELLULAR MEMBRANE - A kit for treating a health condition in a mammal, comprises a ERP57 protein and/or compound for inducing a translocation of an ERP57 protein to a cellular membrane in order to provoke an immunogenic apoptosis. The ERP57 protein may include any one or more of: endogenous ERP57, recombinant ERP57, and ERP57 in mimetic form. The endogenous form of ERP57 may include any one of: a plasma membrane ERP57 and an intracellular ERP57. | 01-01-2009 |
20090004172 | SERVICE FOR EFFECTING LOCALIZED, NON-SYSTEMIC AND SYSTEMIC, IMMUNOGENIC TREATMENT OF CANCER USING ERP57 TRANSLOCATION - Anthracyclines induce the rapid, pre-apoptotic translocation of ERP57 to the cell surface. Knock down of ERP57 inhibit the translocation of CRT, suppressed the phagocytosis of anthracyclines-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. In contrast, the blockade of ERP57 with blocking antibody had no effect on phagocytosis of anthracyclines-treated tumor cells by dendritic cells and their immunogenicity in mammals, such as mice. The anthracyclines-induced ERP57 translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex. Administration of recombinant ERP57 did not restored the immunogenicity of cell death elicited by etoposide and mitomycin C, or enhanced their antitumor effects in vivo in contrast to the administration of recombinant CRT. These data identify the presence of ERP57 crucial for the translocation of CRT and to induce immunogenic cell death which will activate a anti-cancer immune responses. | 01-01-2009 |
20090004178 | PHARMACEUTICAL COMPOUND FOR BLOCKING THE CRT OR ERP57 TRANSLOCATION - A pharmaceutical compound is used in the treatment of a health condition in a mammal. The compound comprises an antibody that interferes with an increased translocation of a protein, leading to an increased immunogenicity of cell death. The antibody may be, for example, anti-calreticulin and/or anti-ERP57. This antibody includes any one or more of blocking or neutralizing antibody. | 01-01-2009 |
20090004211 | METHOD FOR EFFECTING LOCALIZED, NON-SYSTEMIC AND SYSTEMIC, IMMUNOGENIC TREATMENT OF CANCER USING ERP57 TRANSLOCATION - Anthrocyclines-treated tumor cells are particularly effective in eliciting an anti-cancer immune response, where the rDNA-damaging agents, such as etoposide and mitomycin C do not induce immunogenic cell death. Anthracyclines induce the rapid, pre-apoptotic translocation of ERP57 to the cell surface. Knock down of ERP57 inhibit the translocation of CRT, suppressed the phagocytosis of anthracyclines-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. In contrast, the blockade of ERP57 with blocking antibody had no effect on phagocytosis of anthracyclines-treated tumor cells by dendritic cells and their immunogenicity in mammals, such as mice. The anthracyclines-induced ERP57 translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex. Administration of recombinant ERP57 did not restore the immunogenicity of cell death elicited by etoposide and mitomycin C, or enhanced their antitumor effects in vivo, in contrast to the administration of recombinant CRT. These data identify the presence of ERP57 crucial for the translocation of CRT and to induce immunogenic cell death which will activate a anti-cancer immune responses. | 01-01-2009 |
20090004678 | METHOD FOR SCREENING FERTILITY AND NEW COMPOUNDS OR MOLECULES, USING CRT OR ERP57 TRANSLOCATION - A screening method for testing the immunogenicity of new molecules and compounds and for testing fertility and sterility conditions. The method includes inducing a translocation of a calreticulin protein and/or an ERP57 protein, to a cellular membrane in order to determine the immunogenicity of the new molecules and compounds, or the fertility or sterility conditions. The method includes also the using of recombinant CRT and/or ERP57 to treat sterility. | 01-01-2009 |
20090005302 | METHOD, APPARATUS, AND COMPOUND FOR EFFECTING LOCALIZED, NON-SYSTEMIC, IMMUNOGENIC TREATMENT OF CANCER - Anthracyclin-treated turn or cells are particularly effective in eliciting an anti-cancer immune response, where the rDNA-damaging agents, such as etoposide and mitomycin C do not induce immunogenic cell death. Anthracyclins induce the rapid, pre-apoptotic translocation of calreticulin (CRT) to the cell surface. Blockade or knock down of CRT suppressed the phagocytosis of anthracyclin-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. The anthracyclin-induced CRT translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex. Administration of recombinant CRT or inhibitors of protein phosphatase1/GADD34 restored the immunogenicity of cell death elicited by etoposide and mitomycin C, and enhanced their antitumor effects in vivo. These data identify CRT as a key feature determining anti-cancer immune responses and delineate a possible strategy for immunogenic chemotherapy. | 01-01-2009 |
20090005305 | SERVICE FOR EFFECTING LOCALIZED, NON-SYSTEMIC AND SYSTEMIC, IMMUNOGENIC TREATMENT OF CANCER USING CRT TRANSLOCATION - Anthracyclines-treated tumor cells are particularly effective in eliciting an anti-cancer immune response, where the rDNA-damaging agents, such as etoposide and mitomycin C do not induce immunogenic cell death. Anthracyclines induce the rapid, pre-apoptotic translocation of calreticulin (CRT) to the cell surface. Blockade or knock down of CRT suppressed the phagocytosis of anthracyclines-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. The anthracyclines-induced CRT translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex. Administration of recombinant CRT or inhibitors of protein phosphatase1/GADD34 restored the immunogenicity of cell death elicited by etoposide and mitomycin C, and enhanced their antitumor effects in vivo. These data identify CRT as a key feature determining anti-cancer immune responses and delineate a possible strategy for immunogenic chemotherapy. | 01-01-2009 |
20090010952 | PHARMACEUTICAL COMPOUND FOR EFFECTING LOCALIZED, NON-SYSTEMIC AND SYSTEMIC, IMMUNOGENIC TREATMENT OF CANCER USING CRT OR ERP57 TRANSLOCATION - Anthracyclines-treated tumor cells are particularly effective in eliciting an anti-cancer immune response, where the rDNA-damaging agents, such as etoposide and mitomycin C do not induce immunogenic cell death. Anthracyclines induce the rapid, pre-apoptotic translocation of calreticulin (CRT) and/or ERP57 to the cell surface. Knock down of CRT and/or ERP57 suppressed the phagocytosis of anthracyclines-treated tumor cells by dendritic cells and abolished their immunogenicity in mammals, such as mice. The anthracyclines-induced CRT and/or ERP57 translocation was mimicked by inhibition of the protein phosphatase1/GADD34 complex. Administration of recombinant colreticulin, and not recombinant ERP57, or inhibitors of protein phosphatase1/GADD34 restored the immunogenicity of cell death elicited by etoposide and mitomycin C, and enhanced their antitumor effects in vivo. These data identify calreticulin and/or ERP57 as a key feature determining anti-cancer immune responses and delineate a possible strategy for immunogenic chemotherapy. | 01-08-2009 |
20090048159 | KIT FOR TREATING A HEALTH CONDITION BY INDUCING TRANSLOCATION OF A CALRETICULIN PROTEIN TO A CELLULAR MEMBRANE - A kit for treating a health condition in a mammal comprises a calreticulin protein and/or compound for inducing a translocation of a calreticulin protein to a cellular membrane in order to provoke an immunogenic apoptosis. The calreticulin protein may include any one or more of: endogenous calreticulin, recombinant calreticulin, and calreticulin in mimetic form. The endogenous form of calreticulin may include any one of: a plasma membrane calreticulin and an intracellular calreticulin. | 02-19-2009 |
20110060120 | IMMUNOGENIC TREATMENT OF CANCER BY PEPTIDES INDUCING THE PLASMA MEMBRANE EXPOSURE OF ERP57 - We have recently identified (a) ectocalreticulin as the main source of immunogenicity of cancer cell death induced by chemotherapy or radiotherapy, (b) ectoERP57 as critical protein for inducing cell surface exposure of calreticulin, and (c) that ectoERP57 and ectocalreticulin are cotranslocated together to the tumor cell surface by the mediator of the inhibition of PP1/GADD34 complex. Here, I show the design of a peptide that inhibits the interaction between PP1 and GADD34 complex. These inhibitor peptide (a) induce ectocalreticulin and ectoERP57 in a variety of tumor cell lines by the mediator of the inhibition of the interaction between PP1 and GADD34, (b) increase the phagocytosis of anticancer targeted proapoptotic peptide and chemotherapy-treated tumor cells by dendritic cells, and (c) improve highly the anticancer activity of proapoptotic peptides and chemotherapy by suppressing or reducing the tumor growth in several isogenic mouse models of colon, mammary, and fibrosarcoma tumors and by increasing the lifespan of transgenic adenocarcinoma mouse prostate mice. These results suggest that these targeted peptides combination approach could serve as a new powerful autonomous anticancer therapy. | 03-10-2011 |